Effect of basal ganglia calcification on its glucose metabolism and dopaminergic function in idiopathic hypoparathyroidism. (27th November 2014)

• Record Type: Journal Article
• Authors: Modi, Sagar; Arora, Geetanjali; Bal, Chandra Shekhar; Sreenivas, Vishnubhatla; Kailash, Suparna; Sagar, Rajesh; Goswami, Ravinder
• Is Part Of: Clinical endocrinology. Volume 83:Number 4(2015:Oct.)
• Page Start: 563
• Page End: 571
• Publication Date: 2014-11-27
• Subjects: Endocrinology -- Periodicals; 616.4005
• DOI: 10.1111/cen.12649
• Languages: English
• ISSNs: 0300-0664

Abstract

<abstract abstract-type="main" id="cen12649-abs-0001"> <title>Summary</title> <sec id="cen12649-sec-0001" sec-type="section"> <title>Background</title> <p>The functional significance of basal ganglia calcification <bold>(</bold>BGC) in idiopathic hypoparathyroidism (IH) is not clear.</p> </sec> <sec id="cen12649-sec-0002" sec-type="section"> <title>Objective</title> <p>To assess the effect of BGC on glucose metabolism and dopaminergic function in IH.</p> </sec> <sec id="cen12649-sec-0003" sec-type="section"> <title>Methods</title> <p> <sup>18</sup>F‐FDG and <sup>99m</sup>Tc‐TRODAT‐1 nuclear imaging were performed in 35 IH patients with (<italic>n</italic> = 26) and without (<italic>n</italic> = 9) BGC. Controls were subjects without hypoparathyroidism or BGC (nine for <sup>18</sup>F‐FDG and 12 for <sup>99m</sup>Tc‐TRODAT‐1). Relationship of the glucose metabolism and dopaminergic function was assessed with the neuropsychological and biochemical abnormalities.</p> </sec> <sec id="cen12649-sec-0004" sec-type="section"> <title>Results</title> <p> <sup>18</sup>F‐FDG uptake in IH patients with calcification at caudate and striatum was less than that of IH patients without calcification (1·06 ± 0·13 <italic>vs</italic> 1·24 ± 0·09, <italic>P</italic> = <0·0001 and 1·06 ± 0·09 <italic>vs</italic> 1·14 ± 0·08, <italic>P</italic> = 0·03, respectively). <sup>18</sup>F‐FDG uptake did not correlate with neuropsychological dysfunctions. <sup>18</sup>F‐FDG uptake in IH without BGC was significantly lower than that of controls. The mean <sup>99m</sup>Tc‐TRODAT‐1 uptake at basal ganglia was comparable between IH with and without BGC and between IH without BGC and controls. Serum calcium–phosphorus ratio maintained by the patients correlated with <sup>18</sup>F‐FDG uptake at striatum (<italic>r</italic> = 0·57, <italic>P</italic> = 0·001). For every 0·1 unit reduction in calcium–phosphorus ratio, <sup>18</sup>F‐FDG uptake decreased by 2·5 ± 0·68% (<italic>P</italic> = 0·001).</p> </sec> <sec id="cen12649-sec-0005" sec-type="section"> <title>Conclusion</title> <p>BGC was associated with modest reduction (15%) in <sup>18</sup>F‐FDG uptake at basal ganglia in IH but did not affect dopaminergic function. <sup>18</sup>F‐FDG uptake did not correlate with neuropsychological dysfunctions. Interestingly, chronic hypocalcaemia–hyperphosphataemia also contributed to reduction in <sup>18</sup>F‐FDG uptake which was independent of BGC.</p> </sec> </abstract>